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长链非编码 MELTF 反义 RNA 1 通过靶向 miR-1299 促进和预测非小细胞肺癌的进展。

Long non-coding MELTF Antisense RNA 1 promotes and prognosis the progression of non-small cell lung cancer by targeting miR-1299.

机构信息

Department of Pharmacy, The Second Hospital of Jilin University, Changchun, Jilin, China.

Department of Thoracic Surgery, The Second Hospital of Jilin University, Changchun, Jilin, China.

出版信息

Bioengineered. 2022 Apr;13(4):10594-10604. doi: 10.1080/21655979.2022.2063563.

DOI:10.1080/21655979.2022.2063563
PMID:35441579
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9161893/
Abstract

This paper explored the influence of long non-coding MELTF Antisense RNA 1 (lncRNA MELTF-AS1) on the prognosis of non-small cell lung cancer (NSCLC), and further deepened the understanding of NSCLC. A total of 130 patients with NSCLC participated in current study to detect and compare lncRNA MELTF-AS1 expression in cancer and normal tissues. Kaplan-Meier analysis and log-rank test were chosen to analyze the effect of MELTF-AS1 expression on the survival of patients within 5 years. The correlation between the expression of MELTF-AS1 and the clinical characteristics of NSCLC patients was analyzed, and the prognostic factors of NSCLC were analyzed by multivariate Cox regression. Subsequently, MELTF-AS1 expression in NSCLC cells were detected. The Cell Counting Kit-8 (CCK-8) and Transwell methods were selected to study the proliferation, migration capability and invasion level of NSCLC cells that silencing MELTF-AS1. Through the luciferase activity assay to explore the relationship between MELTF-AS1 and miR-1299, to further understand the effect of silencing MELTF-AS1 on NSCLC. MELTF-AS1 was increased in NSCLC tissues and cells. Silencing MELTF-AS1 suppressed the proliferation ability, migration capability and invasion level of NSCLC cells, which means that low expression of MELTF-AS1 may be more conducive to patient survival. In addition, through luciferase activity analysis and bioinformatics analysis, MELTF-AS1 has a negative effect on miR-1299, and silencing MELTF-AS1 enhanced miR-1299 expression in NSCLC cells. MELTF-AS1 is highly likely to be a promising prognostic biomarker, and associated with the progression of NSCLC.

摘要

本文探讨了长链非编码 MELTF 反义 RNA 1（lncRNA MELTF-AS1）对非小细胞肺癌（NSCLC）预后的影响，进一步加深了对 NSCLC 的认识。本研究共纳入 130 例 NSCLC 患者，检测并比较了癌组织和正常组织中 lncRNA MELTF-AS1 的表达。采用 Kaplan-Meier 分析和对数秩检验分析 MELTF-AS1 表达对 5 年内患者生存的影响。分析 MELTF-AS1 表达与 NSCLC 患者临床特征的相关性，采用多因素 Cox 回归分析 NSCLC 的预后因素。随后检测 NSCLC 细胞中 MELTF-AS1 的表达。选择细胞计数试剂盒-8（CCK-8）和 Transwell 法研究沉默 MELTF-AS1 对 NSCLC 细胞增殖、迁移能力和侵袭水平的影响。通过荧光素酶活性测定探讨 MELTF-AS1 与 miR-1299 的关系，进一步了解沉默 MELTF-AS1 对 NSCLC 的影响。MELTF-AS1 在 NSCLC 组织和细胞中表达增加。沉默 MELTF-AS1 抑制了 NSCLC 细胞的增殖能力、迁移能力和侵袭水平，这意味着 MELTF-AS1 的低表达可能更有利于患者的生存。此外，通过荧光素酶活性分析和生物信息学分析，MELTF-AS1 对 miR-1299 有负向作用，沉默 MELTF-AS1 增强了 NSCLC 细胞中 miR-1299 的表达。MELTF-AS1 很可能是一种有前途的预后生物标志物，与 NSCLC 的进展相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/dc3ebd2bd3eb/KBIE_A_2063563_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/f72329f6ca2e/KBIE_A_2063563_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/e91b35a06a63/KBIE_A_2063563_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/f01059cadc83/KBIE_A_2063563_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/748bf8483190/KBIE_A_2063563_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/6055ca4925b6/KBIE_A_2063563_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/dc3ebd2bd3eb/KBIE_A_2063563_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/f72329f6ca2e/KBIE_A_2063563_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/e91b35a06a63/KBIE_A_2063563_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/f01059cadc83/KBIE_A_2063563_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/748bf8483190/KBIE_A_2063563_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/6055ca4925b6/KBIE_A_2063563_F0004_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c9a/9161893/dc3ebd2bd3eb/KBIE_A_2063563_F0005_OC.jpg

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